The focus of this investigation is to determine if specific structural changes in a particular class of cell surface carbohydrate, termed the complex asparagine-linked oligosaccharides, correlate with changes in cell tumorigenicity. Several studies suggest indirectly that this correlation exists, but no precise structural information is known. This project will first compare in detail the complex asparagine-linked (Asn-linked) oligosaccharides on baby hamster kidney cells and their polyoma-virus transformants using sequential lectin-affinity chromatography, a newly devised method of separating the oligosaccharides of interest. Structural determinations will be performed by methylation analyses, before and after glycosidase digestions, using high-performance liquid chromatography to separate the methylated derivatives. Second, the lectin, L-phytohemagglutinin, L-PHA, will be used to select for PyBHK cells that are resistant to this lectin and therefore express altered complex Asn-linked oligosaccharides. L-PHA specifically binds to the highly branched Asn-linked oligosaccharides, the structures that have been implicated to change as cell tumorigenicity increases. After the oligosaccharide structural changes expressed by these L-PHA-resistant cells and the metabolic defects that cause these changes are identified, these cells and the parental PyBHK cells will be separately injected into hamsters. The rates that these cells form tumors will be measured, and the tumors that are formed will be removed and their complex Asn-linked oligosaccharides analyzed. These experiments will test the correlation between the expression of specific Asn-linked oligosaccharides and cell tumorigenicity. In addition, the experiments should determine whether cells with a specific oligosaccharide phenotype are selected from the population of injected cells for survival in vivo, or whether oligosaccharide changes occur in cells after injection, as has been suggested. If a correlation between cell surface oligosaccharide structures and cell tumorigenicity can be substantiated, then experimental strategies can be designed to test how the expression of these specific structures effects changes in the rates that cells form tumors.